Changes in endotoxin levels in T2DM subjects on anti-diabetic therapies.
Changes in endotoxin levels in T2DM subjects on anti-diabetic therapies.
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DOI：
10.1186/1475-2840-8-20
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发表时间：
2009-04-15
影响因子：
9.3
通讯作者：
Harte AL
中科院分区：
文献类型：
--
作者：
Al-Attas OS;Al-Daghri NM;Al-Rubeaan K;da Silva NF;Sabico SL;Kumar S;McTernan PG;Harte AL
慢性低度炎症是肥胖相关糖尿病发生的重要因素。最近的研究表明，源自肠道菌群的内毒素可能通过刺激脂肪组织分泌不利的细胞因子谱而成为炎症发展的关键，这一点得到了支持。该研究调查了内毒素与糖尿病患者各种代谢参数之间的关系，以确定抗糖尿病治疗是否对内毒素水平和脂肪细胞因子谱产生显着影响。空腹血样采集自同意的沙特阿拉伯患者（BMI：30.2 ± (SD)5.6 kg/m2，n = 413），其中包括非糖尿病患者（ND：n = 67）和 T2DM 受试者（n = 346）。根据 1 年治疗方案，糖尿病患者被分为 5 个亚组：饮食控制 (n = 36)、二甲双胍 (n = 141)、罗格列酮 (RSG：n = 22)、二甲双胍/罗格列酮联合固定剂量 (met/RSG n = 100) 和胰岛素 (n = 47)。测定血脂、空腹血糖、胰岛素、脂联素、抵抗素、TNF-α、瘦素、C反应蛋白（CRP）和内毒素浓度。回归分析显示内毒素水平与甘油三酯之间存在显着相关性（R2 = 0.42；p < 0.0001）； T2DM 受试者的总胆固醇（R2 = 0.10；p < 0.001）、葡萄糖（R2 = 0.076；p < 0.001）和胰岛素（R2 = 0.032；p < 0.001）。内毒素与 HDL-胆固醇呈强烈负相关（R2 = 0.055；p < 0.001）。此外，与 ND 相比，所有治疗的糖尿病亚组的内毒素水平均升高，RSG 治疗的糖尿病患者的内毒素水平显着低于所有其他治疗组（ND：4.2 ± 1.7 EU/ml，RSG：5.6 ± 2.2 EU/ml）。 met/RSG 和 RSG 治疗组的脂联素水平均显着高于所有其他组，其中 RSG 组的脂联素水平总体最高。我们得出的结论是，T2DM 的亚临床炎症可能部分是由循环内毒素介导的。此外，虽然接受不同疗法治疗的糖尿病患者的内毒素和脂肪细胞因子谱具有可比性，但 RSG 组在脂联素和内毒素水平上表现出显着差异。我们证实内毒素与血清胰岛素和甘油三酯之间存在关联，而与高密度脂蛋白呈负相关。 RSG 治疗组内毒素降低和脂联素升高可能相关，并表明 RSG 对胰岛素敏感性影响的另一种机制。
Chronic low-grade inflammation is a significant factor in the development of obesity associated diabetes. This is supported by recent studies suggesting endotoxin, derived from gut flora, may be key to the development of inflammation by stimulating the secretion of an adverse cytokine profile from adipose tissue. The study investigated the relationship between endotoxin and various metabolic parameters of diabetic patients to determine if anti-diabetic therapies exerted a significant effect on endotoxin levels and adipocytokine profiles. Fasting blood samples were collected from consenting Saudi Arabian patients (BMI: 30.2 ± (SD)5.6 kg/m2, n = 413), consisting of non-diabetics (ND: n = 67) and T2DM subjects (n = 346). The diabetics were divided into 5 subgroups based on their 1 year treatment regimes: diet-controlled (n = 36), metformin (n = 141), rosiglitazone (RSG: n = 22), a combined fixed dose of metformin/rosiglitazone (met/RSG n = 100) and insulin (n = 47). Lipid profiles, fasting plasma glucose, insulin, adiponectin, resistin, TNF-α, leptin, C-reactive protein (CRP) and endotoxin concentrations were determined. Regression analyses revealed significant correlations between endotoxin levels and triglycerides (R2 = 0.42; p < 0.0001); total cholesterol (R2 = 0.10; p < 0.001), glucose (R2 = 0.076; p < 0.001) and insulin (R2 = 0.032; p < 0.001) in T2DM subjects. Endotoxin showed a strong inverse correlation with HDL-cholesterol (R2 = 0.055; p < 0.001). Further, endotoxin levels were elevated in all of the treated diabetic subgroups compared with ND, with the RSG treated diabetics showing significantly lower endotoxin levels than all of the other treatment groups (ND: 4.2 ± 1.7 EU/ml, RSG: 5.6 ± 2.2 EU/ml). Both the met/RSG and RSG treated groups had significantly higher adiponectin levels than all the other groups, with the RSG group expressing the highest levels overall. We conclude that sub-clinical inflammation in T2DM may, in part, be mediated by circulating endotoxin. Furthermore, that whilst the endotoxin and adipocytokine profiles of diabetic patients treated with different therapies were comparable, the RSG group demonstrated significant differences in both adiponectin and endotoxin levels. We confirm an association between endotoxin and serum insulin and triglycerides and an inverse relationship with HDL. Lower endotoxin and higher adiponectin in the groups treated with RSG may be related and indicate another mechanism for the effect of RSG on insulin sensitivity.
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